The major goals of this application are to evaluate intracellular mechanisms which permit PRL, E, and P to affect TH activity in TIDA neurons. Aim 1 will address the potential role of phosphorylation of TH during conditions of elevated PRL. Protein kinases which affect TH as a response to PRL will be studied. The second aim will examine the mechanisms by which E alters TH activity in a fetal hypothalamic cell culture system. The investigations will determine whether E alters TH mRNA levels. The third aim will focus on acute inhibitory effects of P on TH activity in the fetal hypothalamic cultured cells, and will address the question of whether P can induce dephosphorylation of TH.